Portal de Periódicos da CAPES

Artigo Produção Nacional Revisado por pares

BIBTEX RIS

Varicella-Zoster related vasculopathy as a frequently overlooked cause of stroke

2015; Elsevier BV; Volume: 357; Linguagem: Inglês

10.1016/j.jns.2015.08.1436

1878-5883

Hector Barbosa, Paulo Henrique Sampaio, Clara Barreira, Octávio Marques Pontes‐Neto,

Autoimmune Neurological Disorders and Treatments

Background and objectives: Varicella-Zoster Virus (VZV) is a neurotropic human herpes-virus. Primary VZV infection causes varicella. Later in life, VZV may reactivates, causing zoster, which may manifest with vasculopathy, including stroke and TIA.Case reports: A 42-yo man presented neurological deficits three weeks after zoster in right V2-V3 trigeminal branches and C2-dermatome. MRI findings: bilateral pontine stroke and right trigeminal ganglia enhancement; normal angiogram. CSF was positive for IgG antibody. IV acyclovir was administered, and clinical improvement was substantial. A healthy 18 months old child developed a transitory braquiocrural hemiparesis after chickenpox. MRI showed ischemia in left putamen, coroa radiada and left MCA-M2 branch thickening. CSF findings were normal. Follow-up MRI showed resolution of vasculopathy. No antiviral treatment was administered. Suitable approval for case report was obtained.Discussion: VZV vasculopathy should be suspected in patients with new onset neurological symptoms after zoster. However, it can occur from weeks to months after zoster, and, in some cases, rash is absent. Imaging findings includes both white and gray matter lesions, predominantly in the gray-white matter junction. CSF shows mild mononuclear pleocytosis and elevated erythrocytes. Protein levels are generally elevated, with normal glucose. CSF anti-VZV IgG is more sensitive than VZV DNA test. Treatment is based on IV acyclovir. Steroids therapy benefit has not been established yet.Conclusion: VZV vasculopathy is a potentially treatable vasculitis, although frequently underdiagnosed and with diverse clinical features. Facing VZV high prevalence, it may have an important role in both child and adult stroke. Background and objectives: Varicella-Zoster Virus (VZV) is a neurotropic human herpes-virus. Primary VZV infection causes varicella. Later in life, VZV may reactivates, causing zoster, which may manifest with vasculopathy, including stroke and TIA. Case reports: A 42-yo man presented neurological deficits three weeks after zoster in right V2-V3 trigeminal branches and C2-dermatome. MRI findings: bilateral pontine stroke and right trigeminal ganglia enhancement; normal angiogram. CSF was positive for IgG antibody. IV acyclovir was administered, and clinical improvement was substantial. A healthy 18 months old child developed a transitory braquiocrural hemiparesis after chickenpox. MRI showed ischemia in left putamen, coroa radiada and left MCA-M2 branch thickening. CSF findings were normal. Follow-up MRI showed resolution of vasculopathy. No antiviral treatment was administered. Suitable approval for case report was obtained. Discussion: VZV vasculopathy should be suspected in patients with new onset neurological symptoms after zoster. However, it can occur from weeks to months after zoster, and, in some cases, rash is absent. Imaging findings includes both white and gray matter lesions, predominantly in the gray-white matter junction. CSF shows mild mononuclear pleocytosis and elevated erythrocytes. Protein levels are generally elevated, with normal glucose. CSF anti-VZV IgG is more sensitive than VZV DNA test. Treatment is based on IV acyclovir. Steroids therapy benefit has not been established yet. Conclusion: VZV vasculopathy is a potentially treatable vasculitis, although frequently underdiagnosed and with diverse clinical features. Facing VZV high prevalence, it may have an important role in both child and adult stroke.